The Experts below are selected from a list of 47748 Experts worldwide ranked by ideXlab platform

Michael Schiek - One of the best experts on this subject based on the ideXlab platform.

  • Automated electrical stimulation and recording for Retina implant research by LabVIEW configured standalone data acquisition device
    2014 Proceedings of the SICE Annual Conference (SICE), 2014
    Co-Authors: R. Heil, Mario Schloesser, Andreas Offenhäusser, Stefan Van Waasen, Michael Schiek
    Abstract:

    To understand the neural processes within Retina Cell layers recent Retina implant research focusses on bidirectional communication with bi-polar and ganglion Cells in in-vitro Retinal tissue. In order to enable this research we had developed a front-end to stimulate and record Retinal Cell layers with a slight time gap only and thus avoiding long recording dead times. To ease experiments with this front-end, we developed a versatile and user optimized embedded data acquisition device, named iNODE5. This can be configured using a LabVIEW based graphical user interface. We adapted the front-end to the form factor of the commercial measurement device USB-6009OEM from National Instruments. Now, for evaluation and parameter testing the front-end can be plugged into the National Instruments board and controlled via a graphical user interface which enables the export of the basic configuration parameters for later automated standalone measurement and stimulation. For this the front-end is attached to the iNODE5 which reads the experiment configuration from the personal computer via USB or SD-card. The automated electrical stimulation and recording can be started or stopped by a terminal program or a button placed on the iNODE5.

  • Automated electrical stimulation and recording for Retina implant research by LabVIEW configured standalone data acquisition device
    2014 Proceedings of the SICE Annual Conference (SICE), 2014
    Co-Authors: R. Heil, Mario Schloesser, Andreas Offenhäusser, Stefan Van Waasen, Michael Schiek
    Abstract:

    To understand the neural processes within Retina Cell layers recent Retina implant research focusses on bidirectional communication with bi-polar and ganglion Cells in in-vitro Retinal tissue. In order to enable this research we had developed a front-end to stimulate and record Retinal Cell layers with a slight time gap only and thus avoiding long recording dead times. To ease experiments with this front-end, we developed a versatile and user optimized embedded data acquisition device, named iNODE5. This can be configured using a LabVIEW based graphical user interface. We adapted the front-end to the form factor of the commercial measurement device USB-6009OEM from National Instruments. Now, for evaluation and parameter testing the front-end can be plugged into the National Instruments board and controlled via a graphical user interface which enables the export of the basic configuration parameters for later automated standalone measurement and stimulation. For this the front-end is attached to the iNODE5 which reads the experiment configuration from the personal computer via USB or SD-card. The automated electrical stimulation and recording can be started or stopped by a terminal program or a button placed on the iNODE5.

Patricia S Becerra - One of the best experts on this subject based on the ideXlab platform.

  • pigment epithelium derived factor pedf prevents Retinal Cell death via pedf receptor pedf r identification of a functional ligand binding site
    Journal of Biological Chemistry, 2013
    Co-Authors: Preeti Subramanian, Silvia Locatellihoops, Jason Kenealey, Jacqueline T Desjardin, Luigi Notari, Patricia S Becerra
    Abstract:

    The extraCellular pigment epithelium-derived factor (PEDF) displays Retina survival activity by interacting with receptor proteins on Cell surfaces. We have previously reported that PEDF binds and stimulates PEDF receptor (PEDF-R), a transmembrane phospholipase. However, the PEDF binding site of PEDF-R and its involvement in survival activity have not been identified. The purpose of this work is to identify a biologically relevant ligand-binding site on PEDF-R. PEDF bound the PEDF-R ectodomain L4 (Leu159–Met325) with affinity similar to the full-length PEDF-R (Met1–Leu504). Binding assays using synthetic peptides spanning L4 showed that PEDF selectively bound E5b (Ile193–Leu232) and P1 (Thr210–Leu249) peptides. Recombinant C-terminal truncated PEDF-R4 (Met1–Leu232) and internally truncated PEDF-R and PEDF-R4 (ΔHis203–Leu232) retained phospholipase activity of the full-length PEDF-R. However, PEDF-R polypeptides without the His203–Leu232 region lost the PEDF affinity that stimulated their enzymatic activity. Cell surface labeling showed that PEDF-R is present in the plasma membranes of Retina Cells. Using siRNA to selectively knock down PEDF-R in Retina Cells, we demonstrated that PEDF-R is essential for PEDF-mediated Cell survival and antiapoptotic activities. Furthermore, preincubation of PEDF with P1 and E5b peptides blocked the PEDF·PEDF-R-mediated Retina Cell survival activity, implying that peptide binding to PEDF excluded ligand-receptor interactions on the Cell surface. Our findings establish that PEDF-R is required for the survival and antiapoptotic effects of PEDF on Retina Cells and has determinants for PEDF binding within its L4 ectodomain that are critical for enzymatic stimulation.

R. Heil - One of the best experts on this subject based on the ideXlab platform.

  • Automated electrical stimulation and recording for Retina implant research by LabVIEW configured standalone data acquisition device
    2014 Proceedings of the SICE Annual Conference (SICE), 2014
    Co-Authors: R. Heil, Mario Schloesser, Andreas Offenhäusser, Stefan Van Waasen, Michael Schiek
    Abstract:

    To understand the neural processes within Retina Cell layers recent Retina implant research focusses on bidirectional communication with bi-polar and ganglion Cells in in-vitro Retinal tissue. In order to enable this research we had developed a front-end to stimulate and record Retinal Cell layers with a slight time gap only and thus avoiding long recording dead times. To ease experiments with this front-end, we developed a versatile and user optimized embedded data acquisition device, named iNODE5. This can be configured using a LabVIEW based graphical user interface. We adapted the front-end to the form factor of the commercial measurement device USB-6009OEM from National Instruments. Now, for evaluation and parameter testing the front-end can be plugged into the National Instruments board and controlled via a graphical user interface which enables the export of the basic configuration parameters for later automated standalone measurement and stimulation. For this the front-end is attached to the iNODE5 which reads the experiment configuration from the personal computer via USB or SD-card. The automated electrical stimulation and recording can be started or stopped by a terminal program or a button placed on the iNODE5.

  • Automated electrical stimulation and recording for Retina implant research by LabVIEW configured standalone data acquisition device
    2014 Proceedings of the SICE Annual Conference (SICE), 2014
    Co-Authors: R. Heil, Mario Schloesser, Andreas Offenhäusser, Stefan Van Waasen, Michael Schiek
    Abstract:

    To understand the neural processes within Retina Cell layers recent Retina implant research focusses on bidirectional communication with bi-polar and ganglion Cells in in-vitro Retinal tissue. In order to enable this research we had developed a front-end to stimulate and record Retinal Cell layers with a slight time gap only and thus avoiding long recording dead times. To ease experiments with this front-end, we developed a versatile and user optimized embedded data acquisition device, named iNODE5. This can be configured using a LabVIEW based graphical user interface. We adapted the front-end to the form factor of the commercial measurement device USB-6009OEM from National Instruments. Now, for evaluation and parameter testing the front-end can be plugged into the National Instruments board and controlled via a graphical user interface which enables the export of the basic configuration parameters for later automated standalone measurement and stimulation. For this the front-end is attached to the iNODE5 which reads the experiment configuration from the personal computer via USB or SD-card. The automated electrical stimulation and recording can be started or stopped by a terminal program or a button placed on the iNODE5.

Preeti Subramanian - One of the best experts on this subject based on the ideXlab platform.

  • pigment epithelium derived factor pedf prevents Retinal Cell death via pedf receptor pedf r identification of a functional ligand binding site
    Journal of Biological Chemistry, 2013
    Co-Authors: Preeti Subramanian, Silvia Locatellihoops, Jason Kenealey, Jacqueline T Desjardin, Luigi Notari, Patricia S Becerra
    Abstract:

    The extraCellular pigment epithelium-derived factor (PEDF) displays Retina survival activity by interacting with receptor proteins on Cell surfaces. We have previously reported that PEDF binds and stimulates PEDF receptor (PEDF-R), a transmembrane phospholipase. However, the PEDF binding site of PEDF-R and its involvement in survival activity have not been identified. The purpose of this work is to identify a biologically relevant ligand-binding site on PEDF-R. PEDF bound the PEDF-R ectodomain L4 (Leu159–Met325) with affinity similar to the full-length PEDF-R (Met1–Leu504). Binding assays using synthetic peptides spanning L4 showed that PEDF selectively bound E5b (Ile193–Leu232) and P1 (Thr210–Leu249) peptides. Recombinant C-terminal truncated PEDF-R4 (Met1–Leu232) and internally truncated PEDF-R and PEDF-R4 (ΔHis203–Leu232) retained phospholipase activity of the full-length PEDF-R. However, PEDF-R polypeptides without the His203–Leu232 region lost the PEDF affinity that stimulated their enzymatic activity. Cell surface labeling showed that PEDF-R is present in the plasma membranes of Retina Cells. Using siRNA to selectively knock down PEDF-R in Retina Cells, we demonstrated that PEDF-R is essential for PEDF-mediated Cell survival and antiapoptotic activities. Furthermore, preincubation of PEDF with P1 and E5b peptides blocked the PEDF·PEDF-R-mediated Retina Cell survival activity, implying that peptide binding to PEDF excluded ligand-receptor interactions on the Cell surface. Our findings establish that PEDF-R is required for the survival and antiapoptotic effects of PEDF on Retina Cells and has determinants for PEDF binding within its L4 ectodomain that are critical for enzymatic stimulation.

Paola Bovolenta - One of the best experts on this subject based on the ideXlab platform.

  • SFRP1 modulates Retina Cell differentiation through a beta-catenin-independent mechanism.
    Journal of Cell Science, 2003
    Co-Authors: Pilar Esteve, Françoise Trousse, Josana Rodriguez, Paola Bovolenta
    Abstract:

    Secreted frizzled related proteins (SFRPs) are soluble molecules capable of binding WNTS and preventing the activation of their canonical signalling cascade. Here we show that Sfrp1 contributes to chick Retina differentiation with a mechanism that does not involve modifications in the transcriptional activity of β-catenin. Thus, addition of SFRP1 to dissociated Retinal cultures or retroviral mediated overexpression of the molecule consistently promoted Retinal ganglion and cone photoreceptor Cell generation, while decreasing the number of amacrine Cells. Measure of the activity of the β-catenin-responsive Tcf-binding site coupled to a luciferase reporter in transiently transfected Retinal Cells showed that Sfrp1 was unable to modify the basal β-catenin transcriptional activity of the Retina Cells. Interestingly, a dominant-negative form of GSK3β gave similar results to those of Sfrp1 , and a phosphorylation-dependent inhibition of GSK3β activity followed SFRP1 treatment of Retina Cells. Furthermore, retroviral mediated expression of a dominant-negative form of GSK3β induced a Retina phenotype similar to that observed after Sfrp1 overexpression, suggesting a possible involvement of this kinase in SFRP1 function.

  • SFRP1 modulates Retina Cell differentiation through a beta-catenin-independent mechanism.
    Journal of cell science, 2003
    Co-Authors: Pilar Esteve, Françoise Trousse, Josana Rodriguez, Paola Bovolenta
    Abstract:

    Secreted frizzled related proteins (SFRPs) are soluble molecules capable of binding WNTS and preventing the activation of their canonical signalling cascade. Here we show that Sfrp1 contributes to chick Retina differentiation with a mechanism that does not involve modifications in the transcriptional activity of beta-catenin. Thus, addition of SFRP1 to dissociated Retinal cultures or retroviral mediated overexpression of the molecule consistently promoted Retinal ganglion and cone photoreceptor Cell generation, while decreasing the number of amacrine Cells. Measure of the activity of the beta-catenin-responsive Tcf-binding site coupled to a luciferase reporter in transiently transfected Retinal Cells showed that Sfrp1 was unable to modify the basal beta-catenin transcriptional activity of the Retina Cells. Interestingly, a dominant-negative form of GSK3beta gave similar results to those of Sfrp1, and a phosphorylation-dependent inhibition of GSK3beta activity followed SFRP1 treatment of Retina Cells. Furthermore, retroviral mediated expression of a dominant-negative form of GSK3beta induced a Retina phenotype similar to that observed after Sfrp1 overexpression, suggesting a possible involvement of this kinase in SFRP1 function.